Rad51b activity and cell cycle regulation in response to DNA damage in breast cancer cell lines

Phoebe S. Lee, Jun Fang, Lea Jessop, Timothy Myers, Preethi Raj, Nan Hu, Chaoyu Wang, Philip R. Taylor, Jianjun Wang, Javed Khan, Maria Jasin, Stephen J. Chanock

Research output: Contribution to journalArticlepeer-review


Common genetic variants mapping to two distinct regions of RAD51B, a paralog of RAD51, have been associated with breast cancer risk in genome-wide association studies (GWAS). RAD51B is a plausible candidate gene because of its established role in the homologous recombination (HR) process. How germline genetic variation in RAD51B confers susceptibility to breast cancer is not well understood. Here, we investigate the molecular function of RAD51B in breast cancer cell lines by knocking down RAD51B expression by small interfering RNA and treating cells with DNA-damaging agents, namely cisplatin, hydroxyurea, or methyl-methanesulfonate. Our results show that RAD51B-depleted breast cancer cells have increased sensitivity to DNA damage, reduced efficiency of HR, and altered cell cycle checkpoint responses. The influence of RAD51B on the cell cycle checkpoint is independent of its role in HR and further studies are required to determine whether these functions can explain the RAD51B breast cancer susceptibility alleles.

Original languageEnglish (US)
Pages (from-to)135-144
Number of pages10
JournalBreast Cancer: Basic and Clinical Research
StatePublished - Oct 12 2014


  • Breast cancer
  • DNA damage
  • Homologous recombination
  • RAD51B

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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